• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

122 Cards in this Set

  • Front
  • Back
Most sensitive area for triggering cough reflex
Difference in two bronchi
Right primary bronchus is wider, shorter, and more vertical.
Objects usually end up in the right bronchus b/c its an easier pathway.
Bronchi and blood vessels enter the lungs where?
Tissues of the bronchioles
Smooth muscle
No cartilage
The bronchioles supply the alveoli

Bronchi do contain rings of cartilage.
The business area of the lungs.
Small thin air sacs surrounded by a hair net of capillaries.
Most of the walls of the alveoli are made of simple squamous epithelium, called type 1 alveolar cells, Gas exchange takes place through these cells.
Type II alveolar cells
Produce surfactant (lipoprotein) to decrease the surface tension of water in the lungs.
Dust cells
Alveolar macrophages - phagocytize foreign particles and microbes.
Pulmonary ventilation
Takes place by decreasing the pressure inside the thoracic cavity, and allowing atm pressure to force air into lungs.
Thoracic cavity is expanded primarily by the the contraction and lowering of the diaphragm, but is aided by expansion of the chest by contraction of the external intercostal muscles.
Normally a passive process due to the relaxing of the inspiratory muscles and the elastic recoil of the lungs.
Inadequate blood flow to the lungs.
Inadequate air flow to the alveoli.
Major causes of nosocomial infections
Factors that reduce airflow also compromise particle clearance and predispose to infection.
Restricted lung movement and ventilation may arise due to positioning, constricting bandages, CNS depression, and coma.
There is a high rate of pneumonia in hospital patients b/c of impaired ventilation and clearance.
Signs and symptoms of pulmonary disease
Dyspnea - subjective sensation of uncomfortable breathing, or feeling SOB. Can range from mild discomfort after exertion to extreme difficulty breathing at rest.
Dyspnea is usually caused by diffuse and extensive rather than focal pulmonary disease.
What can cause dyspnea?
Dyspnea can be due to airway obstruction so a greater force is needed to provide adequate ventilation.
Constriction or fluid accumulation in the airways can cause a wheezing sound due to air being forced through these airways.
Can be caused by decreased compliance of lung tissue.
Signs of dyspnea
Flaring nostrils
Use of accessory muscles in breathing.
Retraction, or pulling back, of the intercostal spaces.
The attempt to clear the lower respiratory passages by abrupt and forceful expulsion of air.
This is most common when fluid accumulates in the lower airways.
What can cause a cough?
Inflammation of lung tissue.
Increased secretion in response to mucosal irritation - can be caused by inhalation of irritants, or a intrinsic source of mucosal disruption such as tumor invasion of the bronchial wall.
Excessive blood hydrostatic pressure in pulmonary capillaries - pulmonary edema where excess fluid passes into the airways.
Production of bloody sputum.
Usually involves only a small amount of blood loss.
This is not threatening, but can indicate a serious pulmonary disease such as tuberculosis, lung abscess, cancer, or pulmonary infarction.
If sputum is purulent, an infection of lungs or airway is indicated.
Chronic cough
A cough that persists for more than 3 weeks.
In nonsmokers, almost always due to postnasal drainage syndrome, asthma, or gastroesophageal reflux disease.
In smokers, chronic bronchitis is the most common cause, although lung cancer should be considered.
When blood contains a large amount of unoxygenated hemoglobin, it has a dark red-blue color which gives skin a characteristic bluish appearance.
Most cases arise as a result of peripheral vasoconstriction resulting in reduced blood flow, which allows hemoglobin to give up more of its oxygen to tissues - this is referred to as peripheral cyanosis.
This is best seen in the nail beds.
Can be due to a cold environment, anxiety, etc.
Central cyanosis
Can be due to abnormalities of the respiratory membrane, mismatch b/t air flow and blood flow.
Expressed as a ratio of change in ventilation (V) to perfusion (Q), or V/Q ratio.
Pulmonary thromboembolus can cause reduced blood flow and airway obstruction can result in reduced ventilation.
In persons w/ dark skin this can be seen in the whites of the eyes and mucous membranes.
Peripheral cyanosis
Most cases of peripheral cyanosis arise as a result of peripheral vasoconstriction - results in reduced blood flow, which allows hemoglobin to give up more its oxygen to tissues.
Best seen in the nail beds.
When is cyanosis evident, or observable?
In adults, it is not evident until severe hypoxemia is present.
Clinically observable when reduced hemoglobin levels reach 5 g/dl.
Severe anemia and CO poisoning give inadequate oxygenation of tissues w/o cyanosis.
Individuals w/ polycythemia may have cyanosis when oxygenation is adequate.
Where does pain originate?
Originates in the pleurae, airways, or chest wall.
Inflammation of the parietal pleura causes a sharp or stabbing pain when pleura stretches during inspiration - usually localized to an area of the chest wall where a pleural friction rub can be heard.
Common w/ pulmonary infarction due to embolism.
The selective bulbous enlargement of the end of a digit (finger or toe).
Usually painless.
Commonly assoc'd w/ diseases that cause decreased oxygenation such as lung cancer, cystic fibrosis, lung abscess, or congenital heart disease.
Respiratory failure
The inability of the lungs to adequately oxygenate the blood and to clear it of carbon dioxide.
Can be acute such as w/ ARDS or pulmonary embolism, direct injury to the lungs, airways, or chest wall, or indirect due to injury of another body system such as the brain or spinal cord.
Chronic respiratory failure
Due to progressive hypoventilation from airway obstruction or restrictive disease.
Why is respiratory failure always serious? What are some signs and symptoms?
Nervous tissue is highly oxygen-dependent, so see CNS signs and symptoms such as memory loss, visual impairment, drowsiness, and HA due to increased intracranial pressure due to cerebral vasodilation.
Dysnpea is always present, but it may be difficult to detect a change in a chronic patient.
Hypoxic Respiratory Failure
Seen when pO2 falls to or below 60mmHg.
Typically seen in chronic bronchitis and emphysema, in lung consolidation due to bacterial infection, or in lung collapse, pulmonary htn, pulmonary embolism, and ARDS.
Initially, produces HA and nervous agitation, soon followed by a decline in mental activity and confusion.
With a progressive lowering of pO2, more widespread tissue damage and loss of consciousness can be expected.
Brain stem hypoxia and renal hypoxia.
Brain stem hypoxia
In the event of brain stem hypoxia, CNS output to the heart and systemic arterioles can produce circulatory shock.
Renal hypoxia
Renal hypoxia can cause a loss of homeostatic balance and accumulation of wastes to complicate the problem.
Hypoxic-Hypercapnic respiratory failure
When arterial pCO2 (normally 40mmHg), exceeds 45mmHg, a condition called hypercapnia.
Most often, obstructive conditions produce this form of respiratory failure, as can hypoventilation from CNS problems, thoracic cage, or neuromuscular abnormalities.
How does the body attempt to compensate for hypercapnia? What are some of the effects of this condition?
Attempts to compensate include increased heart rate and vasodilation, which produces warm, moist ski.
CNS effects produce muscular tremors, drowsiness and coma.
Hypercapnia also produces acidosis.
Acute respiratory distress syndrome (ARDS)
Rapid and severe onset of respiratory failure characterized by acute lung inflammation and diffuse injury to the respiratory membrane w/ noncardiogenic edema.
Mortality in persons <60 is 40%.
Those over 65 and immunocompromised still have mortality over 60%.
Most survivors have almost normal lung function 1 year after acute illness.
Pathophysiology of ARDS
All disorders causing ARDS acutely injure the respiratory membrane and produce severe pulmonary edema, shunting, and hypoxemia.
Damage can occur directly via aspiration of acidic gastric contents or inhalation of toxic gases.
Damage can occur indirectly from chemical mediators from systemic disorders.
What is the results of ARDS?
Results is massive inflammatory response by the lungs.
Initial injury damages the pulmonary capillary epithelium causing platelet aggregation and intravascular thrombus formation.
Platelets release substances that attract and activate neutrophils.
Damage also activates the complement cascade which also activates neutrophils and the inflammatory response.
Type II alveolar cells are damaged, and surfactant production is decreased - alveoli fill w/ fluid or collapse.
Lungs become less compliant and ventilation decreases.
What is shunting?
Blow flow is normal, but gas exchanged is decreased. V/Q ratio increases: the same effect as if blood were shunting or bypassing the lungs.
Why are neutrophils central to the development of ARDS?
Neutrophils release inflammatory mediators such as proteolytic enzymes, toxic oxygen products, prostaglandins and leukotrienes, and platelet activating factors.
These damage the respiratory membrane and increase capillary permeability allowing fluids, proteins, and blood cells to leak into alveoli causing pulmonary edema and hemorrhage reducing pulmonary ventilation and compliance.
Neutrophils and macrophages also release mediators that cause pulmonary vasoconstriction which can results in pulmonary htn.
Time span of ARDS
After 24-48 hours hyaline membranes form.
After a/b 7 days, fibrosis progressively obliterates the alveoli, respiratory bronchioles and interstitial.
Result is acute respiratory failure.
How can ARDS lead to multiple organ dysfunction syndrome (MODS)?
Chemical mediators often cause widespread inflammation, endothelial damage and increased capillary permeability throughout the body.
This lead to systemic inflammatory response syndrome, which leads to MODS.
Death may not be caused by ARDS alone, but by MODS.
Clinical manifestations of ARDS
Symptoms develop progressively and include hyperventilation -> respiratory alkalosis -> dyspnea and hypoxemia - > metabolic acidosis -> respiratory acidosis -> further hypoxemia -> hypotension -> decreased cardiac output -> and ultimately death.
Evaluation and treatment of ARDS
Diagnosis is based on physical examination, blood gases, and imaging.
Treatment is based on early detection, supportive therapy, and prevention of complications, especially infection.
Mechanical ventilation is often required.
Some studies underway for treatment include prophylactic immunotherapy, Ab's against endotoxins, inhibition of inflammatory mediators, inhalation of NO to reduce pulmonary htn, and surfactant replacement.
Postoperative respiratory failure
Same pathophysiology as ARDS, but usually not as severe.
Smokers are at risk, esp. if they have a pre-existing lung disease.
Also ppl w/ chronic renal failure, chronic hepatic disease, or infection.
Thoracic and abdominal surgeries carry greatest risk.
Individuals usually have a period of hypotension during surgery, and many have sepsis.
Prevention of postoperative respiratory failure
Frequent turning
Deep breathing, or spirometry.
Early ambulation to prevent atelectasis and accumulation of secretions.
Humidification of the air to loosen secretions.
Supplemental oxygen and antibiotics as appropriate.
Respiratory failure may require mechanical ventilation for a long time.
Obstructive pulmonary disease.
Characterized by airway obstruction that is worse w/ expiration. More force is required to expire a given volume of air, or emptying of lungs is slowed, or both.
Most common obstructive diseases are asthma, chronic bronchitis, and emphysema.
Many ppl have chronic bronchitis and emphysema, and together these are often calle chronic obstructive pulmonary disease (COPD).
Main symptom of obstructive pulmonary disease is dyspnea, and the unifying sign is wheezing.
Individuals have increased work of breathing, V/Q mismatching, and a decreased forced expiratory volume.
Most common obstructive diseases
Asthma, chronic bronchitis, and emphysema.
Chronic bronchitis and emphysema together are allied chronic obstructive pulmonary disease, or COPD.
More intermittent and acute than COPD, even though it can be chronic.
Factor that sets it apart from COPD is its REVERSIBILITY.
Occurs at all ages w/ a/b half developing during childhood.
Runs in families, so genetics may play a role.
Major pathological feature is inflammation resulting in hyper responsiveness of the airways.
Major events in an acute asthma attack
Bronchiolar constriction, mucus hypersecretion, and inflammatory swelling.
Exposure to allergens or irritants causes mast cells to release granules and trigger the release of many inflammatory mediators such as histamine, interleukins, immunoglobulins, prostaglandins, and NO.
See vasodilation and increased capillary permeability.
Chemotactic factors attract neutrophils, eosinophils, and lymphocytes to the area causing bronchial infiltration.
Production of thick, tenacious mucus.
Clinical manifestations of asthma
During remission, the individual is asymptomatic and pulmonary function tests are normal.
Often a severe cough.
Wheezing exhalation.
Attacks usually of one to two hours duration, but may be severe and continue for days or even weeks.
Status asthmaticus
If bronchospasms in asthma are not reversed by usual measures, the individual is considered to have severe bronchospasm or status asthmatics.
If this continues it can be life threatening.
Management and treatment of asthma
Avoid triggers such as allergens and irritants.
Acute attacks are treated w/ corticosteroids and inhaled beta-agonists.
Inhaled bronchodilators,
Immunotherapy such as allergy shots.
Chronic management includes regular use of inhaled anti-inflammatory meds such as corticosteroids, chromolyn sodium, or leukotriene inhibitors.
Bronchoconstriction may be a normal means of restricting airflow and intake of irritants and allergens. Their long term use may actually increase exposure to these factors and cause more pronounced and chronic symptoms.
Anti-inflammatory agents have better long term effects.
Pathological changes that cause reduced expiratory air flow.
Does not change markedly over time.
Does not show major reversibility in response to pharmacological agents.
Assoc'd w/ abnormal inflammatory response of the lungs to noxious particles or gases.
Primary cause is smoking, both active and passive.
Other risks include occupational exposures and air pollution and genetic susceptibilities.
Chronic bronchitis
Hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years, usually in winter.
Pathophysiology of chronic bronchitis
Inspired irritants result in inflammation of the airways w/ infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall.
Causes bronchial edema and increases size and number of mucus glands and goblet cells.
Mucus is thick and tenacious, and can't be cleared b/c of impaired ciliary function.
Increases susceptibility to infection and injury.
Airways collapse in early expiration, blocked by mucus, and air is trapped in distal portion of the tract.
Leads to ventilation/perfusion mismatch.
Hypoxemia occurs.
Air trapping prevents respiratory muscles from functioning efficiently (barrel chest), and get hypoventilation and hypercapnia.
Treatment of chronic bronchitis
Best treatment is PREVENTION b/c changes are not reversible.
Cessation of smoking halts progression of the disease.
Bronchodilators, expectorants, and chest physical therapy are used prn.
Chronic oral steroids as a last resort.
Abnormal, permanent enlargement of the gas-exchange airways and destruction of the alveolar walls.
Obstruction results from changes in lung tissue rather than mucus production and inflammation.
Major mechanism is loss of elastic recoil.
Major cause is smoking but also air pollution and childhood respiratory infections.
Primary emphysema linked to an inherited deficiency of the enzyme alpha-1 antitrypsin which inhibits the action of many proteolytic enzymes which can affect lung tissue.
Pathophysiology of emphysema
Begins w/ destruction of the alveolar septa, which eliminates potions of the capillary bed and increases the volume of air in the alveolus.
Inhaled oxidants inhibit the activity of endogenous antiproteases, and stimulate inflammation w/ increased activity of proteases.
See cont'd alveolar loss and loss of elastic recoil.
Expiration becomes difficult.
Hyperinflation of alveoli produce large air spaces called bullae and air spaces adjacent to the pleura called Blebs.
These aren't effective in gas exchange and result in hypoxemia.
Air trapping causes hyper expansion of the chest, which puts respiratory muscles at a mechanical disadvantage - can result in hypoventilation and hypercapnia late in the disease.
Clinical manifestations of emphysema
Barrel chest
Minimal wheezing
Prolonged expiration
Hypoventilation and polycythemia late in the disease.
Treatment of emphysema
Similar to chronic bronchitis
Smoking cessation
Bronchodilating drugs
Antibiotics for acute infections.
Some can benefit from lung reduction surgery or lung transplant.
Prerenal disease
Results from inadequate blood flow to the kidney, which can be caused by decreased intravascular volume, lesions in the renal arteries, or hypotension.
Systemic disorders that decrease urine output.
Renal disease
Results from direct damage to the nephron.
Glomerular disorders.
Tubulointerstitial disorders which are disorders of the medullary tubules and interstitial cells.
Postrenal disease
Commonly due to urinary tract obstruction, which can be caused by kidney stones or tumors of the bladder, ureters, or prostate gland.
Obstructive disorders
Impedes flow proximal to blockage.
Dilates urinary system.
Increases risk for infection.
Compromises renal function.
Anatomic changes are called obstructive uropathy.
Causes of obstruction
Congenital malformations
Abdominal tumor or inflammation or scarring.
Tumor of urinary system or prostate.
Severe pelvic organ prolapse in women.
What does renal obstruction cause dilation of?
Dilation of ureters - hydroureter
Dilation of pelvis and calyces - hydronephrosis
Dilation of both - ureterohydronephrosis.
What can result from renal dilation?
Enlargement and fibrosis of distal nephron in 7 days.
Interference w/ distal and proximal nephron in 14 days.
Damage to glomeruli in 28 days.
Also see reduction in cortex and medulla.
Initial tubular damage decreases the ability to concentrate urine, causing an increase in urine volume.
The affected kidney can't conserve water, sodium, bicarbonate, or excrete potassium or hydrogen ions - leads to metabolic acidosis and dehydration.
Complete renal obstruction can cause?
Complete obstruction can lead to damage to tubules w/in hours, and irreversible w/in 4 weeks.
Partial renal obstruction can cause?
Partial obstruction can lead to permanent impairment of the ability to concentrate urine, resorb bicarbonate, excrete ammonia, or regulate acid-base balance.
How does the body compensate for damage to one kidney?
The body can partially compensate if one kidney is affected by compensatory hypertrophy of the other kidney.
NO increase in number of nephrons, but do see an increase in size of glomerulus and tubules.
This ability to compensate decreases w/ age.
Compensation is reversible if the other kidney recovers.
Postobstructive diuresis
Relief of partial obstruction of both kidneys or complete obstruction of one kidney results in post obstructive diuresis.
Usually mild and restores fluid and electrolyte balance.
Occasionally, can result in urine output of 10L/day.
Can cause dehydration and electrolyte imbalance.
Obstruction of urethra
Affects upper and lower tracts
Partial obstruction can lead to over active bladder and urine retention.
Can back up and cause hydroureter, hydronephrosis, and impaired kidney function.
Urine can be a microbiological growth medium - infection of obstructed kidney can cause further damage and scarring.
How can obstruction of the urethra cause htn?
The renin-angiotensin pathway in acute unilateral obstruction.
Due to water, sodium, and urea retention in chronic bilateral partial obstruction.
Renal calculi
Kidney stones
Masses of crystals, protein, or other substances.
Common cause of obstruction in adults.
Recurrence w/in 10 years is 50%.
Seen more in men.
Less risk if physically active and drink adequate water.
Calcium oxalate or phosphate is most common stone type.
What can cause renal caliculi?
Get increased concentrations of stone forming molecules in the urine w/ increased renal excretion of these molecules due to increased blood levels, decreased urine volume, and a change in urine pH.
Alkaline urine increases risk of calcium phosphate stones.
Acidic urine increases risk of uric acid stones.
Clinical manifestations of renal caliculi
Pain (renal colic) can determine location.
Nausea and vomiting
Chills and fever
Treatment of renal caliculi
UA and analysis of stones.
Removal by surgery - percutaneous lithotripsy.
Drugs to dissolve stones.
Prevention of renal caliculi/future caliculi
Treat underlying metabolic disorders.
Water intake = urine output of 2-3L/day.
Reduction in dietary oxalates and animal protein for uric acid stones.
Increased dietary fiber.
Do NOT decrease calcium intake - this increases risk of stones.
Inflammation of the bladder
Symptoms of cystitis
Urinary frequency
dysuria - painful or difficult urination.
Lower abdominal, lower back or suprapubic pain.
What is the cause of most UTI's?
Gram negative bacteria of the intestinal tract
80% by E.coli - can form pili allowing bacterium to adhere to bladder epithelium
Cranberry and blueberry juice decreases bacterial adhesions by epicatechin.
Treatment of UTI
Drink normal amounts of water, but avoid bladder irritants, such as caffeine.
Nonbacterial cystitis
Same symptoms but w/o infection.
Dysfunction of external sphincter, urethritis, or inflammation of glands near the vagina.
Interstitial cystitis
May be due to an autoimmune reaction, mucus deficiency, or abnormal mast cells.
Two major functions of the kidneys
Filtration of blood - removes metabolic wastes especially nitrogen containing waste.
Regulation of blood volume and composition, electrolytes, blood pH, and blood pressure.
Functions in filtration, tubular reabsorption, and tubular secretion.
Consists of the renal corpuscle, proximal convoluted tubule, nephron loop of Loop of Henle, distal convoluted tubule, and collecting duct.
Renal corpuscle
In the nephron, the capillary containing glomerulus in the glomerular or Bowman's capsule.
Bowman's capsule receives filtrate.
Proximal convoluted tubule
Reabsorption of water and solutes.
Nephron loop or Loop of Henle
Regulate concentration of urine
Distal convoluted tubule and collecting duct
Reabsorption of water and electrolytes
Tubular secretion
Affected by ADH, aldosterone, and ANP.
juxtaglomerular apparatus
Juxtaglomerular cells lie in the wall of the afferent arteriole.
Macula densa in final portion of the Loop of Henle monitors sodium and chloride concentrations as well as water.
Controls blood flow into the glomerulus and also glomerular filtration.
By the end of the proximal tubule, what has been absorbed?
60-70% of water and sodium
About 100% of glucose and amino acids
90% of potassium, bicarbonate, calcium, and uric acid.
Blood urea nitrogen (BUN)
Urea is produced by the breakdown of amino acids.
If the GFR decreases due to renal disease, renal blockage, or decreased blood flow to the kidney, the BUN increases.
Creatinine clearance
Creatinine is an end product of muscle metabolism.
An indirect measure of GFR and renal blood flow.
Creatinine is neither reabsorbed or secreted, just freely filtered., so the amount excreted equals the amount filtered.
Tubulointerstitial disorders
Acute pyelonephritis
Urinary obstruction and reflux of urine are the most common risk factors.
Can involve one or both kidneys.
Most common in women.
Usually by ascending micro-organisms, but can be carried in blood.
May also be due to effects of drug and toxins.
Acute pyelonephritis
A tubulointerstitial disorder
Inflammation is usually focal and affects the renal pelvis, calyces, and medulla.
Glomeruli usually NOT involved.
Kidney is infiltrated w/ WBC's - pyuria.
Healing involves scarring and atrophy of affected tubules.
Clinical manifestations of acute pyelonephritis
Acute onset
Fever or chills
Flank or groin pain
Dysuria and frequencey.
To distinguish from cystitis - LOOK FOR WHITE CELL CASTS.
Treatment w/ specific antibiotics.
Chronic pyelonephritis
More likely in patients w/ reflux or renal stones.
Scarring can lead to impaired urine-concentrating ability, leading to chronic renal failure.
May be due to drug toxicity from analgesics, such as aspirin, phenacetin, or acetaminophen.
Severe htn is often a contributing factor.
Clinical manifestations of chronic pyelonephritis
Often minimal and include htn, frequency and dysuria, and flank pain.
Diagnosis by UA or intravenous pyelography, ultrasound.
Treatment is to relieve obstruction and antibiotics.
Glomerular disorders
Due to a change or dysfunction of the glomerular capillaries
See changes in membrane permeablilty, GFR, protein or blood cells in urine.
Systemic changes include htn, edema, and acid-base and electrolyte imbalances.
Most commonly caused by an ABNORMAL IMMUNE RESPONSE.
Can be diffuse, focal, or segmental.
Can be membranous, proliferative, sclerotic, or crescentic.
Acute glomerulonephritis
Abrupt onset 7-12 days after strept throat or skin infection (impetigo).
Can also be caused by staphylococcus or viruses.
Strep antigens deposit in glomerular basement membrane and attract neutrophils and macrophages, initiating phagocytosis and release of inflammatory mediators that damage cells on BOTH sides of the basement membrane.
Symptoms of acute glomerulonephritis
Dcreased GFR, oliguria or anuria
Edema around eyes, feet, and ankles.
Ascites or pleural effusion.
Rapidly progressive GN
Primarily adults in 50's and 60's.
May be idiopathic or associated w/ a proliferative disease.
Renal insufficiency by the time of diagnoses.
Proliferation of cells in Bowman's space w/ crescent formation.
Hematuria is common and may also see proteinuria, edema or htn.
Goodpasture syndrome
Antibody formation against pulmonary and glomerular capillary basement membranes.
Activation of complement and neutrophils damages glomerular basement membrane.
Primarily men 20-30 years old.
Can cause pulmonary hemorrhage and renal failure.
Treatment of Goodpasture syndrome
Treatment must begin early or prognosis is poor.
Anticoagulants reduce fibrin content of crescents.
Plasmapheresis w/ steroids and immunosuppression therapy
Chronic glomerulonephritis
Several diseases w/ a progressive course leading to chronic renal failure.
Two patters - deposition of antigen-antibody complexes, or antigens specific for GBM.
Complement activation and phagocyte activity damage capillary walls and cause proliferation of extracellular matrix, affecting GFR.
Clinical manifestations of chronic GN
Initially see increased membrane permeability and lose cells (hematuria) or protein into urine (proteinuria).
Fibrin is deposited into Bowman's space - crescent formation.
Renal blood flow and GFR is reduced.
Hematuria - smoky brown-tinged urine as opposed to pink or red.
Decreased GFR leads to fluid retention and htn.
Renal insufficiency progresses to renal failure after 10-20 years.
Treatment of chronic GN
Treat underlying disease
Steroids do NOT change the course of the disease.
Correct accompanying problems such as volume and b/p disorders.
Ultimately dialysis or transplant.
Nephrotic syndrome
Defined as excretion of 3.5 or more grams of protein per day.
Characteristic of glomerular injury.
Also see hypoalbuminemia, edema, hyperlipidemia
Loss of immunoglobulins can increase susceptibility to infections
Treatment of Nephrotic syndrome
Low-fat and salt restricted diet, but normal protein.
Protein supplements
Removal of glomerular membrane toxic factor.
Nephritic syndrome
Alteration of filtration leads to loss of RBC's.
Also see decreased GFR which causes decreased urine output, azotemia (increased nitrogenous wastes in the blood), and renal tubules undergo disuse atrophy and scarring.
Most common cause of acute renal failure
Prerenal is the most common cause.
Failure to restore blood volume or b/p and oxygen levels can lead to acute tubular necrosis or acute cortical necrosis.
Intrarenal acute renal failure
Usually due to acute tubular necrosis.
Usually caused by ischemia most often after surgery.
Whatever the case, get decreased GFR and oliguria.
Postrenal acute renal failure
Usually due to urinary tract obstruction that affects both kidneys.
Characterized by several hours of anuria w/ flank pain, followed by polyuria.
Three stages of acute renal failure
Stage 1 - Oliguria
Stage 2 - Diuresis
Stage 3 - Recovery
Stage 1 of ARF
Urine volume a/b 25% of normal to anuria.
Increased BUN and plasma creatinine.
Increased potassium (hyperkalemia) and electrolyte imbalance.
Fluid retention and edema
Congestive heart failure
Stage 2 of ARF
3-4 L/day of urine
Tubules still damaged, but recovering,
Can lose too much sodium and potassium and may see extracellular volume depletion
Stage 3 of ARF
May take 3-12 months for plasma creatinine to return to normal.
A/b 30% never regain norma kidney function.
Treatment of Acute renal failure
Prevention if possible
Correct fluid and electrolyte imbalances
Treat infections
Maintain nutrition and cardiac function
Chronic renal failure
Progressive and irreversible loss of nephrons.
Alterations in salt and water balance not apparent until renal function is less than 25% of normal.
Common causes include chronic GN and chronic pyelonephritis.
Clinical manifestations of chronic renal failure
Often described w/ the term uremia - symptoms due to accumulation of toxins in plasma.
htn, anorexia, anemia, edema, pruritis (itching), CV disease, weight loss.
Diagnoses of chronic renal failure
Diagnosis is by increased BUN and serum creatinine.
Imaging will show small kidneys
Management includes restricting proteins and potassium in the diet, evaluating fluid and sodium levels.
Treatment w/ erythropoietin as needed.